# Measurement of oxygen consumption rate in mouse aortic tissue

**Authors:** Zhen Zhou, Ripon Sarkar, Jose Emiliano Esparza Pinelo, Alexis Richard, Jay Dunn, Zhao Ren, Callie S Kwartler, Dianna M Milewicz

PMC · DOI: 10.1093/biomethods/bpaf031 · Biology Methods & Protocols · 2025-04-24

## TL;DR

This study develops a reliable method to measure mitochondrial respiration in mouse aortic tissue, helping understand the metabolic changes in aortic diseases.

## Contribution

The paper introduces an optimized protocol for measuring mitochondrial oxygen consumption in mouse aortic tissue using the Seahorse XFe24 analyzer.

## Key findings

- The protocol enables precise measurement of baseline OCR and responses to mitochondrial inhibitors in mouse aortic tissue.
- The method provides a reproducible approach for assessing mitochondrial function in aortic tissues.
- This technique offers a foundation for studying metabolic shifts in aortic diseases like thoracic aortic aneurysm and dissection.

## Abstract

Thoracic aortic aneurysm and dissection (TAD) is a life-threatening vascular disorder, and smooth muscle cell mitochondrial dysfunction leads to cell death, contributing to TAD. Accurate measurements of metabolic processes are essential for understanding cellular homeostasis in both healthy and diseased states. While assays for evaluating mitochondrial respiration have been well established for cultured cells and isolated mitochondria, no optimized application has been developed for aortic tissue. In this study, we generate an optimized protocol using the Agilent Seahorse XFe24 analyzer to measure mitochondrial respiration in mouse aortic tissue. This method allows for precise measurement of mitochondrial oxygen consumption in mouse aorta, providing a reliable assay for bioenergetic analysis of aortic tissue. The protocol offers a reproducible approach for assessing mitochondrial function in aortic tissues, capturing both baseline OCR and responses to mitochondrial inhibitors, such as oligomycin, FCCP, and rotenone/antimycin A. This method establishes a critical foundation for studying metabolic shifts in aortic tissues and offers valuable insights into the cellular mechanisms of aortic diseases, contributing to a better understanding of TAD progression.

## Linked entities

- **Chemicals:** FCCP (PubChem CID 3330), rotenone (PubChem CID 6758), antimycin A (PubChem CID 14957)
- **Species:** Mus musculus (taxon 10090)

## Full-text entities

- **Diseases:** mitochondrial dysfunction (MESH:D028361), vascular disorder (MESH:D002561), TAD (MESH:D000784), aortic diseases (MESH:D001018)
- **Species:** Mus musculus (house mouse, species) [taxon 10090]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12054972/full.md

## References

25 references — full list in the complete paper: https://tomesphere.com/paper/PMC12054972/full.md

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Source: https://tomesphere.com/paper/PMC12054972